Endocrinology- DM Flashcards
Define Diabetes
- Fasting glucose ≥ 125 after on 2 occasions
- A randome glucose ≥ 200
- An A1c ≥ 6.5
Signs Symptoms of DM
Polyuria Polydipsia Polyphagia Decreased wound healing Candida Infections Weight loss Blurry vision or Self Correcting Presbyopia
What antibodies are present in DM1?
Antibodies to glutamic acid decarboxylase (GAD)
What can falsely decrease HbA1c?
Hemmoglobinopathies: Sickle cell, G6PD, Thalassemia
What is the first treatment for DM2?
MOA, ADR, and contraindications?
BITx: Metformin + Lifestyle (weight loss, exercise, diet)
MOA: blocks gluconeogensis and intestine glucose absorption
ADR: lactic acidosis, B12 deficiency, weight loss
Contas: renal failure, alcoholics, ketoacidosis
DM2 Tx: Sulfanylureas
- names
- moa
- adr
- contraindications
Name: Glyburide, Glipizide. Analogues (Repaglinide, Nateglinide)
MOA: Block ATP-K channels of the pancreatic β cells → depolarization→ insulin secretion
ADR: Weight gain, hypoglycemia, disulfiram-like reaction
Contraindications: Severe cardiovascular, obesity, sulfa-allergy; Analogues: liver failure
DM2 Tx: DPP-4 inhibitors
- names
- moa
- adr
- contraindications
Names: -gliptin (sitagliptin, saxagliptin)
MOA: inhibiting the DPP-4 → less break down GLP-1 & GIP → insulin secretion, ↓ glucagon secretion, delayed gastric emptying
ADR: GI, risk pancreatitis, UTI (mild) , URI
Contras: Liver failure, kidney failure
DM2 Tx: SGLT2 inhibitors
- names
- moa
- adr
- contraindications
Names: -glifozin (empaglifozin, dapaglifozin)
MOA: inhibition of SGLT-2 in the PCT of kidney → ↓ glucose reabsorption → glycosuria and polyuria
ADR: UTI (significant), fungal vaginitis, dehydration, DKA
Contras: CKD, recurrent UTI.
use after 2-3 other oral dont work
DM2 Tx: Thiazolidinesiones
- names
- moa
- adr
- contraindications
Name: -glitazones (Pioglitazone, Rosiglitazone)
MOA: activation PPARγ → ↑ transcription of genes → ↑ adiponectin and insulin sensitivity → ↑ storage of fatty → ↓ free fatty acids → ↑ glucose utilization and ↓ hepatic glucose production
ADR: Weight gain, osteoporosis, risk of heart failure, edema & fluid retention.
Contras: no clear benefit; CHF; Liver failure
DM2 Tx: GLP-1 agonist
- names
- moa
- adr
- contraindications
Names: -tide (exenatide, liraglutide); semaglutide (first oral GLP agonist )
MOA: Bind to the GLP-1 receptors → ↑ insulin secretion, ↓ glucagon secretion, slow gastric emptying (↑ feeling of satiety, ↓ weight)
ADR: GI (slow gastric motility), weight loss, Pancreatitis
Conrats: symptomatic GI, Hx or FHx of pancreatitis or cancer
DM2 Tx: Alpha glucosidase inhibitors
- names
- moa
- adr
- contraindications
Names: acarbose, miglitol
MOA: Inhibit alpha-glucosidase → delayed and ↓ intestinal glucose absorption (post prandial control)
ADR: Flatus, diarrhea, abd pain,
Contras: IBD, malabsorption
Characteristics of insulin: rapid acting
- names
- onset
- peak
- duration
- application
Names: Lispro, Aspart, glulisine (LAG)
Onset: 5-15 min
Peak: 1hr
Duration: 3-4 hrs
Application: basal bous; sliding scale
Characteristics of insulin: short acting
- names
- onset
- peak
- duration
- application
Name: Regular
Onset: 30-60min
Peak: 2hrs
Duration: 6-8hrs
Application: hyperglycemic emergency (only IV insulin), insulin pumps, sliding scale
Characteristics of insulin: intermediate acting
- names
- onset
- peak
- duration
- application
Name: NPH (Neutral protamine Hegedron)
Onset: 2-4 hrs
Peak: 6-7hrs
Duration: 10-16hrs
Application: glucocorticoid hyperglycemia, resistant DM2,
Characteristics of insulin: Long acting
- names
- onset
- peak
- duration
- application
Names: glargine, detemir, degludec
Onset: 1-4 hrs
Peak: Flat- no peak
Duration: 24-36hrs
Application: Basal bolus regiment
Time adjustment for NPH and regular insulin:
7am glucose issue
12pm glucose issue
5pm glucose issue
9pm glucose issue
To correct a 7am problem adjust NPH at dinner the night before.
To correct 12pm: adjust Regular morning dose
To correct 5pm: adjust NPH morning dose
To correct 9pm: adjust Regular dinner dose.
Somogyi Effect
Too much insulin at dinner –> overnight hypoglycemia –> morning release stress hormone –> 7am high glucose.
Tx: decrease evening insulin
Dawn phenomenon
Hyperglycemia caused by growth hormone early in the am.
Elevated 7am glucose no overnight hypoglycemia.
Tx: increase evening glucose
What is DKA?
Diabetic Ketoacidosis is an acute hyperglycemic, hyperosmolar state typically in type 1 diabetics with metabolic acidosis (due to hepatic ketone production), and hyperkalemia.
Deadly without treatment.
What is HHS/NKHS
Non ketotic hyperglycemic hyperosmolar Syndrome occurs only in type 2 diabetics at much higher glucose levels. There is no ketones or acidosis due to small levels of insulin production.
What signs/ symptoms are specific to DKA?
Polyuria Polydipsia Volume depletion Neuro (AMS, lethargy, coma) Rapid onset (< 24 h) Abdominal pain Fruity odor(from exhaled acetone) Kussmaul respirations Hyperkalemia w/ decreased total body K Metabolic acidosis with anion gap Low Bicarb
What signs/ symptoms are specific to HHS?
Polyuria/ Polydipsia Recent weight loss Nausea and vomiting Neuro (AMS, lethargy, coma) Severly profound dehydration Slower onset (over days) Glucose >600 Normal Anion gap and Bicarb Increased risk seizure
Tx DKA
first: Large volume fluids and short acting insulin
Replace K as levels approach normal.
Correct underlying cause.
What is the mechanism of ketoacidosis in DKA?
Insulin deficiency → ↑ lipolysis → ↑ free fatty acids → hepatic ketone production (ketogenesis) → ketosis → bicarbonate consumption (as a buffer) → anion gap metabolic acidosis
What is the mechanism of total potassium deficit in DKA?
Insulin deficiency →
hyperosmolality →
K shift out of cells + no insulin for K uptake →
intracellular K depleted & elevated blood K levels
Which is the best measure of the severity in DKA?
Serum Bicarb (anion gap)
as anion gap increases risk of death increase, regardless of glucose level.
What is the mortality rate of DKA and HHS?
DKA 10% with current treatment
HHS 50% if mental status change at start of treatment
Tx HHS
Due to severe dehydration: FLUIDS FLUIDS FLUIDS
second: insulin and electrolyte replacement
Health maintenance for diabetic patients
Pneumococcal vaccine Annual eye exam (retinopathy) ACE/ ARB if >140/90 or +microalbuminuria Statin therapy LDL >100 Foot Exams Microalbuminuria test annually
What are the most common long term complications of DM?
Cardiovascular complications Retinopathy Nephropathy Vascular disease Neuropathy Risk of infection
Cardiovascular complications in DM
MI (most common cause of death in DM)
Silent MI (painless due to neuropathy)
Stroke
CHF
Goal BP <140/90, LDL <100
Diabetic nephropathy
DM #1 cause of ERDS requiring HD
Microalbuminuria early disease
ACE/ ARB slow and prevent
Diabetic retinopathy
DM leading cause of blindness due to microvascular damage.
Proliferative retinopathy: neovascularization and virtuous hemorrhages.
Tx Diabetic retinopathy
Proliferative retinopathy is treated with pan retinal laser photocoagulation.
Vascular endothelial growth facto (VEGF) inhibitors treat severe retinopathy
Diabetic neuropathy
Damage to microvasculature damages the vasa nervorum that surrounds peripheral nerves.
Neuropathy with pain: pregabalin, gabapentin, TCA
Risk of infection in DM
WBC don’t function well in hyperglycemic environment. Decreses sensation and PAD cannot deliver WBC to site of early infection.
What problems can result from diabetic neuropathy?
Gastroparesis Charcot Joints Impotence Cranial Nerve Palsies Orthostatic hypotension Foot injuries
DM gastroparesis
Immobility os the bowel due to decreased ability to sense stretch of bowel walls.
Bloating, constipation, early satiety, vomiting
Tx gastroparesis
Metoclopramide
erythromycin
Unresponsive: gastric pacemaker
Charcot Joints
Joints of the foot and ankle deform secondary to lack of sensation. Pts may brake a bone and not feel it
Impotence in DM
caused by vascular atherosclerosis and neuropathy
Cranial nerve palsies in DM
Microvascular ischemia of Daniela nerves especially CN 3,4,6.
Facial nerve palsy simile to Bell palsy
Orthostatic hypotension in DM
Arteries dont “clamp down” when the patients stands up and HR fails to increase
How should you manage diabetic patients who are not allowed to eat because they are scheduled for surgery?
1/3 to 1/2 normal insulin dose.
Close glucose monitoring intra and post-op
Beta blockers, hypoglycemia and diabetics?
BB mask classic symptoms of hypoglycemia which are caused by catecholamine release.
With Hx of previous MI, benefits outweigh risk of using a BB.
What should be remembered before giving IV iodinated contrast to a diabetic?
DMs are prone to acute renal failure from IV iodine contrast. No concern with oral contract.
Weigh risks and benefits.
Administer IV fluids prior to contrast.
Decrease risk with acetylcystine and bicarb.
IV iodinated contrast and metformin
Risk for lactic acidosis is acute renal failure were to accuse with IV contrast. Pts with advanced CKD or AKI should have metformin held before contrast and 48hrs after contrast.
Hypoglycemia and DM
most common cause for hospitalization
MCC: inappropriate dose adjustment
Tx: glucose and/or glucagon
Other causes of hypoglycemia
Insulinoma
Insuline autoimmune antibodies
Sulfonylurea Abuse
Serruptitious use of insulin/ suicide.
When should a diabetic foot ulcer be imaged for osteomyelitis?
Deep ( exposed bone, probe to bone) Long standing ( >7-14 days) Large (>2cm) Elevated ESR/ C-reactive protein Adjacent soft tissue infection ( not always evident due to neuropathy and poor immune response)
Elevated A1c with moral fasting glucose
post prandial hyperglycemia
Management of post prandial hyperglycemia
Basial-Bolus insulin
Basal and Rapid acting
